| Literature DB >> 25214401 |
Yuyan Han1, Paolo Onori2, Fanyin Meng3, Sharon DeMorrow4, Julie Venter1, Heather Francis3, Antonio Franchitto5, Debolina Ray1, Lindsey Kennedy6, John Greene7, Anastasia Renzi2, Romina Mancinelli2, Eugenio Gaudio2, Shannon Glaser8, Gianfranco Alpini9.
Abstract
Biliary hyperplasia and liver fibrosis are common features in cholestatic liver disease. Melatonin is synthesized by the pineal gland as well as the liver. Melatonin inhibits biliary hyperplasia of bile duct-ligated (BDL) rats. Since melatonin synthesis (by the enzyme serotonin N-acetyltransferase, AANAT) from the pineal gland increases after dark exposure, we hypothesized that biliary hyperplasia and liver fibrosis are diminished by continuous darkness via increased melatonin synthesis from the pineal gland. Normal or BDL rats (immediately after surgery) were housed with light-dark cycles or complete dark for 1 wk before evaluation of 1) the expression of AANAT in the pineal gland and melatonin levels in pineal gland tissue supernatants and serum; 2) biliary proliferation and intrahepatic bile duct mass, liver histology, and serum chemistry; 3) secretin-stimulated ductal secretion (functional index of biliary growth); 4) collagen deposition, liver fibrosis markers in liver sections, total liver, and cholangiocytes; and 5) expression of clock genes in cholangiocytes. In BDL rats exposed to dark there was 1) enhanced AANAT expression/melatonin secretion in pineal gland and melatonin serum levels; 2) improved liver morphology, serum chemistry and decreased biliary proliferation and secretin-stimulated choleresis; and 4) decreased fibrosis and expression of fibrosis markers in liver sections, total liver and cholangiocytes and reduced biliary expression of the clock genes PER1, BMAL1, CLOCK, and Cry1. Thus prolonged dark exposure may be a beneficial noninvasive therapeutic approach for the management of biliary disorders.Entities:
Keywords: biliary epithelium; cholestasis; clock genes; melatonin; secretin
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Year: 2014 PMID: 25214401 PMCID: PMC4216989 DOI: 10.1152/ajpgi.00288.2014
Source DB: PubMed Journal: Am J Physiol Gastrointest Liver Physiol ISSN: 0193-1857 Impact factor: 4.052